Abstract
Helicobacter pylori is a Gram-negative pathogen that can increase the risk of stomach cancer in infected patients. H. pylori exploits lipid rafts to infect host cells. Infection triggers clustering of Lewis x antigen (Lex) and integrins in lipid rafts to facilitate H. pylori adherence to the gastric epithelium. H. pylori infection can be treated with probiotics containing lactic acid bacteria that offer numerous benefits to the host while lacking the side effects associated with antibiotic therapy. Previously, we showed that the cell-free supernatant (CFS) derived from Lactobacillus rhamnosus JB3 (LR-JB3) at a multiplicity of infection (MOI) of 25 attenuated the pathogenicity of H. pylori. In this study, we established a mucin model to simulate the gastric environment and to further understand the influence of mucin on the pathogenesis of H. pylori. Porcine stomach mucin dramatically upregulated H. pylori virulence gene expression, including that of babA, sabA, fucT, vacA, hp0499, cagA, and cagL, as well as the adhesion and invasion ability of H. pylori and induced increased levels of IL-8 in infected-AGS cells. The CFS derived from LR-JB3 at a MOI of 25 reduced the expression of H. pylori sabA, fucT, and hp0499 in mucin, as well as that of the Lex antigen and the α5β1 integrin in AGS cells during co-cultivation. These inhibitory effects of LR-JB3 also suppressed lipid raft clustering and attenuated Lewis antigen-dependent adherence, type IV secretion system-mediated cell contact, and lipid raft-mediated entry of VacA to host cells. In conclusion, LR-JB3 could affect H. pylori infection through mediating lipid raft formation of the host cells. The currently unknown cues secreted from LR-JB3 are valuable not only for treating H. pylori infection, but also for treating diseases that are also mediated by lipid raft signaling, such as cancer and aging-associated and neurodegenerative conditions.
Highlights
Helicobacter pylori is a Gram-negative pathogen that colonizes the gastric mucosa and increases the risk of stomach cancer in infected patients [1, 2]
After entering the lumen of the stomach, H. pylori moves through the mucus layer to increase the accessibility of adhering to gastric epithelial cells [24]
Antibiotic therapy has limitations including development of antibiotic-resistant strains [34] and disruption of the balance in intestinal microflora, which can lead to gastrointestinal diseases [35]
Summary
Helicobacter pylori is a Gram-negative pathogen that colonizes the gastric mucosa and increases the risk of stomach cancer in infected patients [1, 2]. Lactic acid bacteria are known to offer numerous benefits to the host, including protection against H. pylori infection [5]. We indicated that oral administration of Lactobacillus rhamnosus JB3 (LR-JB3) to mice could eliminate H. pylori infection and attenuate inflammatory responses by suppressing vacA gene expression [6]. LR-JB3 induced superoxide dismutase and catalase activity, and the serum levels of beneficial amino acids, which are impaired by H. pylori infection [7]. These results indicated that LR-JB3 has potential in eliminating H. pylori infection. The mechanism that underlies LR-JB3 activity against H. pylori infection should be further investigated to support potential clinical applications
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